Th17/Treg imbalance in peripheral blood from patients with intracranial aneurysm.

Abstract

Background: Spontaneous subarachnoid hemorrhage (SAH) is highly associated with ruptured intracranial aneurysm (IA), which dramatically increases neurological disabilities or mortality in patients. The balance between T helper cells (Th17) and regulatory T cells (Treg) plays a crucial role in regulating immune-inflammatory response. In the current study, we aim to obtain a better understanding of the role of Th17 and Treg cells in patients with IA.

Methods: 138 patients total participated in this study, including ruptured aneurysms group (Ruptured IA, RIA, N.=70 cases) and unruptured aneurysms group (Unruptured IA, URIA, N.=68 cases). Additionally, 76 cases of healthy subjects were selected as control group. The frequencies of Th17 and Treg cells were determined using flow cytometry. The serum levels of cytokines including IL-17, IL-23, IL-10, and TGF-β1 were determined using ELISA. mRNA was isolated from the whole blood. FOXP3 and RCRc mRNA expressions were detected using RT-qPCR.

Results: The percentage of Th17 cells in peripheral blood from RIA patients was higher than URIA patients (P<0.01), whereas the percentage of Treg cells in peripheral blood from RIA was significantly lower when compared with URIA patients (P<0.001). The serum levels of IL-17 (P<0.01) and IL-23 (P<0.05) were markedly increased while the levels of IL-10 (P<0.01) and TGF-β1 (P<0.05) were decreased in RIA patients when compared with URIA patients. Lastly, the mRNA level of RCRc was significantly increased in RIA vs. URIA patients (P<0.001). By contrast, FOXP3 mRNA level was significantly decreased in RIA vs. URIA patients (P<0.001).

Conclusions: In the current study, we demonstrated the imbalance of Th17/Treg in patients with IA, and the frequencies of Th17 cells were positively correlated with the severity of IA-induced SAH. These results provided data to support that targeting Th17/Treg could act as an effective approach for the management of IA.